Figure 2.

TMEV infection induces CNS-myeloid cell activation and vessel association in the hippocampus. (A) CX3CR1⁺ CNS-myeloid cells (green) in representative hippocampal images from uninfected and TMEV infected (7 dpi) CX3CR1^gfp/+ mice. Zoomed insets demonstrate areas in which CX3CR1⁺ cells cluster around vasculature. n = 3 mice (3 sections/mouse). Scale bars: 100 μm. (B) Density of hippocampal CX3CR1⁺ cells in naïve and TMEV infected mice. (C) Representative images of DAPI (nuclei, blue), CX3CR1 (CNS-myeloid, green), and intravascularly injected dextran (vasculature, red) in the hippocampus of naïve and TMEV-infected mice. n = 3 mice (6 sections/mouse). Scale bars: 25 μm. (D) Quantification of the proportion of CX3CR1⁺ cells in contact with hippocampal vasculature in naïve and infected conditions. (E) Representative images of hippocampal microglial morphology (confocal and transformed skeletal) in uninfected and TMEV infected mice (7 dpi). n = 3 mice (3 sections/mouse). Scale bars: 10 μm. (F) Quantification of hippocampal microglia soma size at 7 dpi TMEV compared to naïve. (G) Sholl analysis of microglia at 7 days post TMEV infection or during steady state. (25 microglia/section, 2 sections/mouse). Area under the curve of the Sholl analysis is used to demonstrate quantification of microglial branching during infection. Data are representative of ≥ 2 independent experiments and presented as mean +/- SD, 2-tailed unpaired Student’s t test with ns p ≥ 0.05.